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Therapeutics > Exam 2 lecture 5 > Flashcards

Exam 2 lecture 5 Flashcards

1
Q

steps for electrical conduction in heart

A
  1. SA node fires (pacemaker cells start beating)
  2. Excitation spreads through atrial myocardium
  3. AV node fire
  4. Excitation spreads down AV bundle
  5. Purkinje fibers distribute excitation through ventricular
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2
Q

PQRST meaning

A

P- beginning
Q- 1st dip
R- highest tip
S- Second dip
T- last beat

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3
Q

P wave is a culmination of

A

SA node, atrium and AV node

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4
Q

QT is determined by

A

Wide action potential mediated by Ca2+

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5
Q

What are some important ion channels in heart

A

Na channels
Calcium channels
K channels
HCN channels
hERG channels

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6
Q

What are the types of Na, Ca, K, HCN and hERG channels in heart

A

Na- Na V 1.5
Ca- N type, CaV 2.2, T type
K- Kir, Kv
HCN- HCN1, HCN 4
hERG- KCNH2, KV 11.1

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7
Q

what is an important channel to avoid targeting when developing new drugs

A

hERG

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8
Q

Membrane concentration of cells inside and outside of cells

A

inside
K- more K inside
Na- less Na inside
Ca- less Ca inside
Cl- less Cl inside

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9
Q

charge inside the cell vs outside the cell numerical value

A

inside- -70mV
outside- 0 mV

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10
Q

explain how an action potential is formed

A

-Na channels open and cause depolarization
-causes a rise in membrane potential
-Na channels close and there is a plateu when Ca cells come into cell and K cells go out of cell (cause contration)
- when Ca channel closes, rapid repolarization occurs

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11
Q

compare pacemaker cells and ventricular myocytes (important)

A

pacemaker cells
-specialized non-contractile cells
-physiologically depolarized
-Ca2+ dependent spikes
ACTION POTENTIAL -50mV
no plateu in image

Ventricular myocytes
- contractile cells
-hyperpolarized
-Na2+ dependent spikes
-86 mV action potential
long plateu phase

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12
Q

how does Ach affect Ca and HCN

A

reduce both

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13
Q

how does Ach affect ion channels

A

cause hyperpolarization and block activation of ion channels (reduce HR)

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14
Q

what are the 3 phases of Na channels in phase 0

A

Rest
open
inactivation

during rest- flat on graph
Open makes it shoot up
inactivation (ball and chain method ball plugs hole) causes a slow decline to rest)

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15
Q

can we form another action potential when channel is inactivated

A

no, it is called the refractory period

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16
Q

phase 2 and 3 of action potential generation

A

K+ channel opens and drives K out
Ca channel brings Ca inside
This causes a plateau
eventually ca channels will be inactivated then most of the force will be mediated by K channels, action potential goes down

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17
Q

Re entry arrhythmia requirements

A
  1. multiple parallel pathway
  2. Unidirectional block
  3. conduction time greater than ERP (effective refractory period)
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18
Q

What are the Antiarrhythmic drugs

A

Class 1- Na channel blockers
Class 2- B adrenergic antagonists
Class 3- K channel blockers (prolong refractory period)
Class 4 Caclium channel blockers

19
Q

Which 2 classes of antiarrhythmic drugs have common features

A

Class 2 and 4 (B adrenergic and Ca2+)

20
Q

Know the difference in how class 2 and class 4 look in EKG

A

Class 2 peaks have the same height
view notebook
CCB causes reduction in peak

21
Q

How do B adrenergic agonists affect HR

A

slow it down

22
Q

how do class 2 anti arrhythmics (BAR blockers) affect pacemakers? Ca currents? PR interval? refractoriness of AV node?

A

slow pacemakers
slow Ca currents
increase PR interval
increase refractoriness of AV node

23
Q

are class IV anti arrythmics (CCBs) frequency dependent blocks

A

yes

24
Q

How do class IV antiarrythmics affect refractoriness of AV node? PR interval? ventricular rate?

A

increase refractoriness of AV node
protects ventricular rate from tachycardia

25
Q

What are some BAR drugs used as antiarrythmics? are they cardio selective or non selective

A

Esmolol (cardioselective)
acebutolol (cardioselective)
propranolol(non-selective)

26
Q

Know the structure of esmolol for exam

A
27
Q

clinical use of BAR drugs

A

arrhythmias involving catecholamines

28
Q

What are the Class IV (CCB) drugs

A

Verapamil
Diltiazem

29
Q

use of diltiazem as antiarrhythmic

A

Block re-entrant arrhythmias involving AV node

30
Q

how to recognize diltiazem and verapamil structures

A

verapamil- has double oxygen on left and right side
Diltiazem- has N and S in structure
Google structure

31
Q

What are the different types of Class 1 antiarrhythmic drugs

A

Class 1A- Mixed block (Na and K)
Class 1B- Na channel blocker
Class 1C- Strong Na blocker

32
Q

What are the different 1A, 1B and 1C drugs

A

1A- Quinidine, procainamide
1B- lidocaine, mexiletine
1C- Flecainide, propafenone

33
Q

Class 1A drug effect on action potential

A

Widen QRS and prolong QT

34
Q

Class 1B drug effect on action potential

A

Has no clinical significance on ECG

35
Q

Class 1C effect on action potential

A

Widen QRS

36
Q

Which states of Na do 1A, 1B and 1C drugs affect

A

Class 1A- blocks open state
Class 1B- Blocks open and inactive state
Class 1C- Blocks open state

37
Q

Class III anti arrythmics MOA

A

K channel blockers

38
Q

How do class III antiarythmics effect ECG

A

prolong action potential duration and QT interval
increase ERP

39
Q

class III drug name

A

Amiodarone
dronedarone
sotalol

40
Q

why is amiodarone important

A

top choice for rate control in A fib, suppression of post MI ventricular arrythmia

41
Q

What are acquired long QT syndromes

A

Genetic mutations (KCNQ1 (potassoum) SCNSA (sodium) cause LQTS

42
Q

where do different classes of antiarrythmics affect the action potential

A

Class 1 affects the first rise (depolarization)
Class 4 affects the plateau
Class 3 affects the repolarization (down graph)
Class 2 affects the very end

43
Q

what are some miscellaneous antiarrythmic drug

A

Digoxin
Adenosine (leads to slowing of heart)

Therapeutics (38 decks)

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